Evidence map›Paper›PMID 27703302›Full record

ArticleMediators of inflammation2016

SOCS1 Mimetic Peptide Suppresses Chronic Intraocular Inflammatory Disease (Uveitis).

Chang He, Cheng-Rong Yu, Mary J Mattapallil, Lin Sun, Joseph Larkin Iii, Charles E Egwuagu

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Tregs in Autoimmune Uveitis.Advances in experimental medicine and biology · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Chang HeMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA; State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China.
Cheng-Rong YuMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Mary J MattapallilImmunoregulation Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Lin SunMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Joseph Larkin IiiDepartment of Microbiology & Cell Science, University of Florida, Gainesville, FL 32611, USA.ORCID 0000-0003-2066-6814
Charles E EgwuaguMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-9986-3839
National Institutes of Health · USUniversity of Florida · US

Funding

Development of Immunologic therapies against uveitisZIAEY000350 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$6.7M
Mechanisms of immune homeostasis and regulation of intraocular inflammationZIAEY000372 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$6.5M
Regulation of JAK/STAT pathways in the eyeZIAEY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$5.4M
Suppressors of Cytokine Signalling (SOCS) have Neuroprotective Roles in RetinaZIAEY000280 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$3.3M
6 · The paper itself

Abstract

Uveitis is a potentially sight-threatening disease characterized by repeated cycles of remission and recurrent inflammation. The JAK/STAT pathway regulates the differentiation of pathogenic Th1 and Th17 cells that mediate uveitis. A SOCS1 mimetic peptide (SOCS1-KIR) that inhibits JAK2/STAT1 pathways has recently been shown to suppress experimental autoimmune uveitis (EAU). However, it is not clear whether SOCS1-KIR ameliorated uveitis by targeting JAK/STAT pathways of pathogenic lymphocytes or via inhibition of macrophages and antigen-presenting cells that also enter the retina during EAU. To further investigate mechanisms that mediate SOCS1-KIR effects and evaluate the efficacy of SOCS1-KIR as an investigational drug for chronic uveitis, we induced EAU in rats by adoptive transfer of uveitogenic T-cells and monitored disease progression and severity by slit-lamp microscopy, histology, and optical coherence tomography. Topical administration of SOCS1-KIR ameliorated acute and chronic posterior uveitis by inhibiting Th17 cells and the recruitment of inflammatory cells into retina while promoting expansion of IL-10-producing Tregs. We further show that SOCS1-KIR conferred protection of resident retinal cells that play critical role in vision from cytotoxic effects of inflammatory cytokines by downregulating proapoptotic genes. Thus, SOCS1-KIR suppresses uveitis and confers neuroprotective effects and might be exploited as a noninvasive treatment for chronic uveitis.

Indexed as

AnimalsAntigen-Presenting CellsBiomimeticsChronic DiseaseFlow CytometryJanus Kinase 2MacrophagesPeptidesRatsSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinTh17 CellsUveitisJak2 protein, ratJanus Kinase 2PeptidesSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 Protein

Identifiers

PMID27703302
PMCPMC5040805
OpenAlexW2519747283

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.